Histological and immunohistochemical study on the effect of zinc oxide nanoparticles on cerebellar cortex of adult male albino rats

Abstract

Background: Zinc oxide nanoparticles (ZnONPs) are one of metal nanoparticles that have widespread use in many fields. Objective: To investigate the effect of ZnONPs on cerebellar cortex of rats through histological and immunohistochemical study. Materials and methods: Thirty adult male albino rats were divided into three groups; group I (control), Group II (ZnONP-1 treated group) which received orally 50 mg/kg of ZnONP for two months and Group III (ZnONP-1I treated group) which received orally 200 mg/kg of ZnONP for two months. Specimens of the cerebellar cortex were processed for histological and immunohistochemical study. Morphometric and statistical analysis were carried out. Results: Group II showed Purkinje cells were crowded in many layers surrounded by perineuronal vacuoles and had pyknotic nuclei. They had cytoplasmic vacuoles and perinuclear Golgi apparatus revealed fragmented dilated cisternae. Nearby Bergmann astrocyte cells had highly vacuolated cytoplasm and the nerve fibers were also affected and showed dysmyleination (disrupted myelin sheath). Immunohistochemical study of the same group showed Purkinje cell cytoplasm had positive immunoreactions for calretinin proteins. In group III, there was a wide spread of neuronal affection to the degree of loss of many of Purkinje cells leaving empty spaces. Ultrastructurly, their cytoplasm appeared with multiple variable sized and had dilated mitochondria with disrupted cristae. The Bergmann astrocytes revealed nuclei with disrupted nuclear envelope and nearly absence their cytoplasmic organelle and there was more affection to the nerve fibers in the form of vacuolated axoplasm and demyelination (areas of myelin loss) beside dysmyleination. Immunohistochemical study of group III showed Purkinje cells cytoplasm with negative immunoreactions for calretinin proteins. Conclusion: Intake of ZnONPs induced various adverse alterations in the histological and immunohistochemical structures of cerebellar cortex indicating the occurrence of neurotoxicity. These changes were exaggerated with increasing the dose of their intake.

Evaluation of the Postnatal Effects Induced by Diazinon on the Growth of the Mice Offspring and the Development of Their Cerebellar Cortex

“…Cells Tissues Organs 2022;211:539-554 DOI: 10.1159/000518993 [2018], who detected them in the granular layer and explained that this finding might result from an increase in oxidative stress and free radicals. Abdel-Aziz et al [2019] and Amin et al [2019] reported a similar finding in Purkinje cells and explained it as an outcome of the failure of the energy-dependent Na+ K+ ion pumps due to induced lipid peroxidation. Zhang et al [2017] and Mohamed and Mohamed [2018] correlated the vacuolations to the degeneration of cell organelles due to oxidative stress, depletion of the antioxidants, and mitochondrial dysfunction.…”

“…Meanwhile, Purkinje cells in group IIa (at birth) were displaced upward in the molecular layer and downward in the granular layer, which is described as multi-layer deposition of Purkinje cells. Azmy and Abd Allah [2013] and Abdel-Aziz et al [2019] reported similar findings and explained them as an adaptive response resulting from neuronal insult.…”

“…They stated that the condensed nuclear chromatin might be an outcome of condensation and dissolution of chromatin of dying neurons. Abdel-Aziz et al [2019] reported that it was secondary to alterations in Purkinje neurons leading to a gradual loss of synchronization between cells. Ali et al [2018] mentioned that the free radical has a crucial role in neural cell damage and the ultrastructural changes were an early stage of apoptosis.…”

“…The myelination's disruption resulting from changes in myelin basic protein led to membrane damage and axonal degeneration. Also, the free radicals potentially damaged the oligodendrocytes (responsible for myelination) and neurons causing cell membrane damage and impairment of myelination [Alizadeh et al, 2015;Abdel-Aziz et al, 2019].…”